Fig. 12.23 ). This purely passive property is due to the elasticity of the muscle tissue. If the muscle is stimulated to contract at these various lengths, a different relationship is obtained. Specifically, contractile force increases as muscle length is increased up to a point (designated LO to indicate optimal length). As the muscle is stretched beyond LO, contractile force decreases. This length-tension curve is consistent with the sliding filament theory, described previously. At a very 0 1 201 Length (fraction of optimum) Sarcomere length (µm) •Fig. 12.23. Length-Tension Relationship in Skeletal Muscle. A, Experimentalsetupinwhichmaximalisometrictetanictensionismeasuredatvariousmusclelengths.B, Howactivetensionwascalculatedatvariousmusclelengths(i.e.,bysubtractingpassivetensionfromtotaltensionateachmusclelength).C, Plotofactivetensionasafunctionofmusclelength,withthepredictedoverlapofthickandthinfilamentsatselectedpoints.
•Fig. 12.24. Force-Velocity Relationship of Skeletal Muscle. Theexperimentalsetupisshownontheright.Theinitialmusclelengthwaskeptconstant,buttheamountofweightthatthemusclehadtoliftduringtetanicstimulationvaried.Whilethesevariousamountsofweightwerelifted,muscle-shorteningvelocitywasmeasured.Seetextfordetails.F,force;V,velocity.
long sarcomere length (3.7 µm), actin filaments no longer overlap with myosin filaments, and so there is no contraction. As muscle length is decreased toward LO, the amount of overlap increases, and contractile force progressively increases. As sarcomere length decreases below 2 µm, the thin filaments collide in the middle of the sarcomere, the actin-myosin interaction is disturbed, and hence contractile force decreases. For construction of the length-tension curves, muscles were maintained at a given length, and then contractile force was measured (i.e., isometric contraction).
Thus the length-tension relationship supports the sliding filament theory of muscle contraction.
The velocity at which a muscle shortens is strongly dependent on the amount of force that the muscle must develop (
Fig. 12.24 ). In the absence of any load, the shortening velocity of the muscle is maximal (denoted as V0). V0 corresponds to the maximal cycling rate of the cross-bridges (i.e., it is proportional to the maximal rate of energy turnover [ATPase activity] by myosin). Thus V0 for fast-twitch muscle is higher than that for slow-twitch muscle. Increasing the load decreases the velocity of muscle shortening until, at maximal load, the muscle cannot lift the load and hence cannot shorten (zero velocity). Further increases in load result in stretching the muscle (negative velocity). The maximal isometric tension (i.e., force at which shortening velocity is zero) is proportional to the number of active cross-bridges between actin and myosin, and it is usually greater for fast-twitch motor units (because of the larger diameter of fast-twitch muscle fibers and greater number of muscle fibers in a typical fast-twitch motor unit). In
Fig. 12.24 , the power-stress curve reflects the rate of work done at each load and shows that the maximal rate of work was done at a submaximal load (namely, when the force of contraction was approximately 30% of the maximal tetanic tension). To calculate the latter curve, the x-and y-coordinates were simply multiplied, and then the product was plotted as a function of the x-coordinate.
1.